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Endocrine > Lec 14 Adrenal III > Flashcards

Lec 14 Adrenal III Flashcards

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1
Q

How common is primary aldosteronism?

A

5-10% of all cases of “essential” hypertension

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2
Q

What are syndromes of apparent mineralocorticoid excess?

A

neither DOC or aldosterone is elevated
- cortisol made in excess or not properly inactivated to cortisone [in 11B-HSD deficiency] and is acting on the mineralocorticoid receptor

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3
Q

What are the actions of aldosterone?

A
  • exchange Na and H for K at distal collecting tubule [DCT]

- increase Na and volume, BP, decrease K [hypokalemia]

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4
Q

What are some things that regulate aldosterone levels?

A
  • RAAS [primary]
  • hyperkalemia
  • ACTH
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5
Q

What is the escape phenomenon?

A

atrial natriuretic factor [ANF} made in heart gets stimulated by high BP and modulates clinical effects of excess mineralocorticoid [aldosterone]

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6
Q

What should you with if high BP and unprovoked hypokalemia or severe diuretic-induced hypokalemia?

A

primary aldosteronism = 50% of cases

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7
Q

What are the two major causes of primary hyperaldosteronism?

A
  • aldosterone producing adenoma [1/3]

- idiopathic hyperaldosteronism [bilateral] [2/3]

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8
Q

What number value tells you primary aldosteronism?

A

high aldosterone in setting of suppressed renin

aldosterone: renin ratio > 20

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9
Q

WHat are characteristics of aldosteronomas?

A

very small; may not be seen on imaging

up to 50% have bilateral disease so have to identify source of excess aldosterone

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10
Q

What is medical therapy for aldosteronoma?

A

aldosterone antagonists [spironolactone or epleronone]

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11
Q

What is familial aldosteronism?

A

recombination of genes encoding CYP11B1 and CYP11B2 –> chimeric gene that encodes hybrid proteins/steroids

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12
Q

What is treatment for familial aldosteronism?

A

suppress ACTH with glucocorticoids [b/c the chimeric gene is under ACTH control]

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13
Q

How do you localize site of aldosteronoma?

A

bilateral adrenal venous sampling; compare ratio

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14
Q

What mutation found in aldosterone producing adenomas?

A

CNJJ5 mutation in gene encoding the K channel

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15
Q

What is adrenal medulla derived from?

A

neuroectoderm –> phechromoblasts

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16
Q

What is the adrenal cortex derived from?

A

true glandular tissue

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17
Q

What is role of adrenal medulla in sympathetic nervous system?

A

serve as amplifiers of SNS

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18
Q

WHat 3 major hormones secreted by adrenal medulla?

A
  • epinephrine
  • norepinephrine
  • dopamine
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19
Q

What is the rate limiting step in steroid hormone production in medulla?

A

conversion of tyrosine to dihydroxyphenlalanine [DOPA] cautalzyed by tyrosine hydroxylase

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20
Q

From what AA are catecholamines synthesized?

A

tyrosine

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21
Q

What converts NE to Epi? What induces it?

A

PNMT [phenylethanolamine N-methyltransferase] converts NE to Epi
induced by cortasol

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22
Q

Does adrenal medulla secrete more epinephrine or NE?

A

secretes 4x more Epi

[NE total circulating levels higher b/c of NE release from postganglionic sympathetic neurons]

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23
Q

What stimulates catecholamine release from adrenal medulla?

A
  • postural changes [supine to standing]
  • low intravascular volume
  • hypoglycemia
  • severe illness
  • emotional stress [fear or rage]
  • tumors [pheochromocytomas and paragangliomas]
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24
Q

What are the major signals for catecholamine release?

Study These Flashcards
A
  • decrease BP, blood volume, or glucose
25
What is epi/NE affinity for a1/a2 receptors?
epi > NE for a1/a2
26
What is epi/NE affinity for B1 receptors?
epi = NE
27
What is epi/NE affinity for b2 receptors?
epi > > > NE | overall effect = increased contractility and vasodilation
28
Do adrenal medulary tumors that hypersecrete primarily Epi cause hypertension or hypotension?
hypotension b/c have super high affinity for B2 which causes vasodilation
29
What things do catecholamines increase?
- blood glucose - lipolysis - skeletal muscle blood flow/contractility - HR - CO - BP
30
What things do catecholamines decrease?
- visceral blood flow - GI motility - urine output
31
What is a pheochromocytoma?
adrenal medullary tumor derived from neural crest = chromaffin cells
32
What is a paraganglioma?
catecholamine secreting tumor arising from sympathetic paraganglion OR extra-adrenal pheochromocytomas
33
What kind of hormones are secreted by paragangliomas?
often don't secrete at all; if they do its NE
34
What kind of hormones are secreted by pheochromocytomas?
NE and/or epi | b/c of high PNMT due to cortisol
35
What is effect of pheochromocytomas?
triad: headache, sweating, palpitations in person with hypertension - blanching - tachycardia - chest pain - arrhythmia - postural hypotension
36
Which pheos are more likely to be malignant?
- extra-adrenal [paraganglioma] - tumors > 6 cm - more dense = > 10 hounsfield units
37
What percent of pheos are associated with familial cause?
> 25%
38
How do you diagnose pheochromocytoma?
- plasma free metanephrines | - 24 hr urine metanephrine
39
What are metanephrines?
metabolites of catecholamines
40
How do you localize where pheochromocytoma is secretin?
MRI T2 = lights up bright highly metabolically active tissue PET scan I-meta-iodobenyzlgunaidine [MIBG] scan
41
What is adrenal incidentaloma?
adrenal mass > 1cm discovered during radiologic exam incidentally > 4cm be suspicious of cancer
42
What percent of adrenal incidentalomas are functional?
10-25%
43
What hormone is primarily secreted by subclinical adrenal incidentalomas?
5-47% secrete cortisol
44
What are the three Ps of MEN1?
- pituitary tumor - parathyroid tumor - pancreatic endocrine tumors
45
What are the 4 genetic syndromes associated with pheochromocytoma?
- nerufibromatosis I - MEN 2a - MEN 2b - Von Hippel Lindau
46
What causes Von Hippel Lindau?
inactivating mutation in VHL tumor suppressor gene
47
What causes MEN1?
autosomal dominant deletion 11q13 = inactivation of tumor suppressor gene MENIN
48
What causes MEN2?
activating RET-proto-oncogene mutation --> activation of receptor tyrosine kinase autosomal dominant
49
What kind of tumors associated with von hippel lindau?
- pheochromocytoma | - renal cell carcinoma
50
What is presentation of MEN2 syndromes?
- pheochromocytomas - hyperparathyroidism [4 gland hyperplasia] - medullary cancer of thyroid
51
What is unique to MEN2B clinical presentation?
marfanoid habitus mucosal neuromas ganglioneuromas
52
What is presentation of MEN1?
- pituitary tumors - pancreatic endocrine tumors [zollinger ellison or insulinoma or glucagonoma] - parathyroid tumors [hyperplasia]
53
What causes neurofibromatosis 1?
mutation in gene encoding parafibromin = tumor suppresso
54
What is presentation of neurofibromatosis I?
- pheochromocytomas - skin neurofibromas - iris hamartomas - cafe au lait spots
55
What is familial paraganglioma syndrome?
mutations in genes encoding succinate dehydrogenase complex --> uncouples mitochondrial e- transport and causes hypoxic state have - pheochromocytomas - paragangliomas can result in malignant and metastatic disease
56
What percent of adrenal incidentalomas are malignant?
< 3%
57
What is the differential diagnosis for bilateral adrenal tumors?
- metastatic disease - congenital adrenal hyperplasia [CAH] - cortical adenomas - lymphoma - infeciton - hemorrhage - ACTH dependent cushing - pheo - amyloidosis
58
What is BMAH?
bilateral macronodular hyperplasia --> causes metabolic syndrome and mild hypercortisolism

Endocrine (21 decks)

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